When grown on high-phosphate medium, the wild-type strain 74A of N. crassa synthesized two acid phosphatases, as shown by DEAE -cellulose chromatography. These purified enzymes showed heterogeneity on PAGE, low specific activities towards PNP-P, molecular weight values of at least 300000, no deviation from Michaelian behaviour, and great stability in 50 mM sodium acetate buffer, at pH 5·4, when kept at 54 °C. These acid phosphatases were synthesized in reduced amounts or not at all when the mould was grown under conditions of phosphate starvation, indicating that the level of phosphate also regulates the synthesis of the high molecular weight enzyme forms. When grown on high phosphate medium, the pho-3 mutant strain also synthesized two acid phosphatases, whose purified enzymes showed no pronounced differences when compared to those synthesized by the wild-type strain in terms of electrophoretic analysis, specific activities towards PNP-P, molecular weight values, and Michaelian behaviour. However, one enzyme form had a higher Km value and a lower heat stability than the corresponding enzyme of the wild-type strain. Even though the pho-3 locus might not be responsible for an alteration in the primary structure of the repressible acid phosphatase, it seems clear that the enzymes synthesized by the mould grown on low-or high-phosphate medium must share some structural features. Thus, the drastic differences observed in the molecular properties of the enzymes synthesized by the mould grown under conditions of phosphate starvation as opposed to phosphate repression might be due to an effect exerted by the level of inorganic phosphate in regulating the translation, post-translational modifications and/or excretion, but not necessarily the gene-directed synthesis of distinct mRNAs.

Recombination between the t6 complex, three allozyme-encoding loci, two antigen-encoding loci, and four molecular markers was studied. The allozyme-encoding loci were complement component-3 (C-3), kidney catalase (Ce-2), and glyoxalase-1 (Glo-1); the antigen-encoding loci were the H-2 Class I genes H-2K and H-2D; the four molecular markers were Tu66, an α-globin pseudogene (Hba-4ps), an unidentified H-2 Class I gene, and the H-2 Class II gene I-Aβ. The latter six loci were used as markers for the t complex. Recombination was detected between Glo-1, Ce-2 and C-3, but not between the markers for the t complex Tu66, Hba-4ps, and the H-2 loci. These data indicate that Ce-2 and C-3 are located outside the t6 complex, while the latter are located within. These data also indicate that the telomeric boundary of the t6 complex is located between H-2 and Ce-2. Recently published studies have shown that complete gametic disequilibrium exists between the t complex and loci located centromeric to the H-2 - Ce-2 interval, while disequilibrium was not detected between loci located telomeric to this interval. Loci included within the region of recombination suppression are also those in disequilibrium with the t complex. As a result, recombination suppression probably resulting from chromosomal rearrangements associated with the t complex appears to be a sufficient explanation for the gametic disequilibrium observed between certain loci and the t complex.

Mutants of Chinese hamster ovary (CHO) cell resistant to cytosine arabinoside (ara-C), an inhibitor of DNA synthesis and antitumour drug, have been isolated and characterized both biochemically and genetically. Mutants occurring spontaneously and those induced by treatment with N-methyl-N′-Nitro-N-nitrosoguanidine (MNG), were obtained at a frequency of 0·24 × 10−6 and 3·4 10−6 respectively. The mutants showed a stable ara-C resistant phenotype which was inherited as a dominant trait in genetic crosses. The wild type (CHO K-1) and the mutant (103, 002 and 003) cells showed no differences in the levels of the uptake of ara-C or of its degradation. Results of biochemical studies further excluded the involvement of deaminase, kinase and ribonucleotide reductase as the possible factor(s) in conferring drug resistance to the mutant cells. However, the wild type and mutant DNA polymerases differed in the level of the in vitro incorporation of specific dNMP in the presence of ara-CTP. These data suggested that the wild-type DNA polymerase which becomes error prone in the presence of ara-CTP may cause the drug sensitivity of the wild-type cells and that a change in the mutant enzyme making it resistant (or less prone) to ara-CTP induced errors in dNMP incorporation may control the drug resistance of the mutant cells.

Data from Neurospora, Drosophila, and the mouse support the mapping parameter conventionally used for man, exclude the Haldane, Kosambi, and Carter—Falconer functions, and suggest a refinement for centromere mapping. Different sexes, chromosome arms, and types of data are surprisingly consistent. Double recombination frequencies are accurately predicted, but triple recombination frequencies are overestimated. The centromere appears to act on interference as an obligatory chiasma. Recombination across the centromere conforms to a simple approximation, based on the interval Markov assumption with a common mapping parameter. These results imply that mapping of n loci requires estimation of at most n parameters, and the relation between map distances and all recombination frequencies is explicit.

Covariance between direct and maternal genetic effects on body weight in random-bred ICR mice at 2 through 10 weeks of age was estimated from cross-fostering experiments. The covariance contributes only a few percent of phenotypic variance at 2 weeks, but increases to 10–15% at later ages. Nearly all estimates are positive. We suggest that genes active during later parts of growth affect maternal performance more than those active during early growth, causing increased covariance at later ages. A model of combined genetic and persistent environmental effects on maternal performance is presented. Persistent effects of genetic or environmental variation in recent ancestors can influence covariance between relatives and response to selection.

The lack of robustness of models of the maintenance of polymorphism in a heterogeneous environment which has been pointed out by Maynard Smith & Hoekstra (1980), applies also to models based on habitat selection, on temporal variation and on density-regulated selection. Only if (partial) dominance ‘switches’ between environments such that the fitness of the heterozygote is always close to the favoured homozygote, is there reasonable robustness. This is true for all models considered. It is argued that there are good reasons for supposing that the favourable allele at a locus may show dominance, although the experimental evidence is still scanty.

Relationships between protein genetic distance (D) and protein heterozygosity (H) were studied using allele frequency data for 42 proteins derived from multilocus electrophoretic surveys of genetic variation in over 200 invertebrate and over 300 vertebrate species. D¯ and H¯ values for the different proteins (mostly enzymes) were calculated, and large and significant correlations between D¯ and H¯ were found in comparisons of both intraspecific and interspecific populations. Empirical relationships between D¯ and H¯ were compared with neutral expectations under the stepwise model of neutral mutation with the assumption that populations are in equilibrium with respect to the effects of mutation and genetic drift.

At low divergence levels, a linear relationship of D¯ on H¯ was observed, but at high levels of divergence D tended towards an asymptote at high H¯. The results at high divergence cannot be explained using the approximate relationship D = 2ut (where u = mutation rate, t = time). However, computer simulations of neutral models showed that changes of this nature in the relationship between D¯ and H¯ were to be expected as divergence increases, the equation D = 2ut being a poor approximation at high D We therefore conclude that the observed relationships between D¯ and H¯ are, in fact, compatible with equilibrium neutral theory.

Chromosomal localization of a gene involved in sisomicin production of Micromonospora rosea n.sp. was suggested by the results of matings between antibiotic producer and non-producer auxotrophic mutants. The frequency of producers among prototrophic recombinants varied with the chromosomal markers used for selection. The sis allele of the parent which was able to overgrow its partner in mixed culture predominated amongst the recombinants.